The nature of consciousness remains deeply mysterious and profoundly important, with existential, medical and spiritual implication. We know what it is like to be conscious – to have awareness, a conscious ‘mind’, but who, or what, are ‘we’ who know such things? How is the subjective nature of phenomenal experience – our ‘inner life’ - to be explained in scientific terms? What consciousness actually is, and how it comes about remain unknown. The general assumption in modern science...

Quick Links

Search form

You are here

Debate with Christof Koch - Heading in the wrong direction

I wrote a review of Christof Koch's book, The quest for consciousness, which appeared in the November (2) issue 2004 of sci-con.org; Christof replied to my critique, with his response appearing in the December (2) issue. In turn, I have responded to Christof's reply, though my response has not yet appeared.

This is a very readable, informative book by a recognized expert and leader in neuroscience / cognitive science related to the problems of consciousness. It also reflects the esteem and affection held by Christof for his collaborator and friend Francis Crick who, sadly, died recently. Many of their mutual ideas are presented in the book which includes thoughtful, extremely useful recapitulations at the end of each chapter. Admirably, Christof embraces the ‘hard problem’, acknowledging as real the issue of how conscious experience in the form of qualia arises from neural activities in the brain. But he avoids an assault, choosing instead to seek the neural correlate of consciousness—the NCC, a term and concept introduced by Crick. “A man’s got to know his limitations” Christof once said about this strategy, quoting Clint Eastwood. Fair enough. Identifying the precise neuronal activity and location which correspond to consciousness would be a gigantic accomplishment. Christof points to a variety of nonconscious activities—Zombie modes—which, he argues, are performed in the guise of consciousness. We merely (falsely) believe we are thinking, analyzing, planning and executing many actions consciously, but we are only actually aware of the final big picture. He relates this concept to Ray Jackendoff’s intermediate theory, in which consciousness is sandwiched between raw sensory percepts and executive planning. I was intrigued by the chronicle of the 40 Hz story. As many people know, Crick and Koch jumpstarted the 40 Hz bandwagon in 1990 with their endorsement of gamma synchrony oscillations (discovered by Lord Adrian, I learned from Christof) popularized by Gray and Singer’s 1985 paper. Borrowing from von der Marlsburg’s notion of correlational binding, Crick and Koch proposed 40 Hz as the NCC, but backed away from it a few years later. In “The quest..” Christof explains that 40 Hz may be useful in promoting a particular coalition of neurons into the lead in competition among coalitions to win the prize of consciousness. But 40 Hz, he says, is not necessary for sustained consciousness. OK, but what is? And what does it mean to be sustained if consciousness is a sequence of discrete events (a property deduced elsewhere in the book)? Likewise the famous “V1 isn’t conscious” story was enlightening. The notion of the back of the brain “looking” at the front of the brain is fascinating. Descriptions of coalitions of neurons forming and dissolving like political alliances is nicely written, although I don’t see much difference between these coalitions and Donald Hebb’s neural assemblies, described a half century ago. Coalitions/assemblies are groups of neurons connected by axonal-dendritic (or axonal-somatic) chemical synapses. Axonal action potentials—spikes—within the coalitions/assemblies are the currency and sine qua non of consciousness, according to Christof. But are they? Cursorily, Christof considers other candidates for the neural-level substrate of the NCC.

He mentions that local field potentials (LFPs) are detectable everywhere in the brain, centimeters from their origin. As a global means of communication, however, he concludes that the LFP electromagnetic field is a “crude and inefficient way for neurons to share information”. Perhaps so, but Christof neglects to consider the source of LFPs (i.e. rather than LFPs themselves) as the NCC. This would be prudent if one believes fMRI to be a good indicator of the NCC. Nikos Logethetis and colleagues showed a few years ago that the BOLD signal in fMRI corresponds with LFPs more so than with axonal spikes. According to Walter Freeman, potentials recorded from scalp or brain surface are not truly LFPs but “open” potentials stemming from dendritic activities of pyramidal cells with axial symmetry. LFPs derive from cortical interneurons with radial symmetry. Which brings us to Christof’s next NCC candidate: “groups of inhibitory cortical neurons linked by….electrical synapses known as gap junctions. Under some conditions all these interneurons trigger action potentials at the same time, acting as a single unit.” But Christof dismisses the possibility: “Not enough is known about this phenomenon to implicate it in conscious perception.” A footnote to the last sentence cites 3 papers showing that cortical interneurons linked by gap junctions generate synchronized activity at around 8 Hz. But actually, in the past 5 years dozens of papers have shown that cortical interneurons linked by gap junctions are responsible for gamma synchrony/40 Hz. The interneurons are linked by dendro-dendritic gap junctions so that membranes are continuous, and depolarize synchronously, “behaving like one giant neuron” as Eric Kandel says in his textbook. The gap junctions are windows between cell interiors so that cell cytoplasm is also continuous. Gap junction networks are, almost literally, one giant neuron (or a “hyper-neuron” as Roy John christened them), but yet as changeable as a Hebbian assembly. Gap junctions may also link dendrites to glia, glia to glia, axons to axons, and axons to dendrites, over-riding chemical synapses. Some thalamo-cortical neurons are also linked by gap junctions in thalamus. The evidence is unclear regarding gap junctions between cortical interneurons and primary (e.g. pyramidal) neurons, but ‘hyper-neurons’ could include primary cortical neurons via direct gap junctions and/or glial bridges including those bypassing chemical synapses. Though far sparser than chemical synapses, electrotonic gap junctions are prevalent significantly in the mature brain. Gap junction hyper-neurons mediate gamma synchrony/40 Hz via cortical interneurons, and may extend widely through cortical and sub-cortical regions. Could they mediate consciousness? Christof continues: “How else but with spikes can the highly peculiar character of any one subjective experience—a subtle shade of pink or a rhapsodic waltz tune—be communicated across multiple cortical and subcortical regions?” This question drips with irony. First, all of a sudden we seem to be tackling the hard problem. Or are we? Does character of qualia imply qualia themselves, or some pertinent information about them? If “the highly peculiar character” of qualia means qualia themselves, then the question should not be “How else but with spikes?” but rather “How in the world can spikes possibly produce qualia?” But if Christof means the latter, that the character of qualia involves non-conscious information about them, then, yes, qualia (“The ball has topspin”) could generate nonconscious instructions by axonal spikes to pre-motor and motor cortex: (“Bend your knees!”). But whither qualia? Whither consciousness? To me the answer is obvious. Consciousness occurs in dendrites, and the results are conveyed elsewhere by axonal spikes. Eccles thought so, and so does Karl Pribram (“Dendrites, dendrites, dendrites!!”) Dendrites are missing in action in “The Quest for Consciousness”. They are barely mentioned. Yet a review in Science characterized dendrites (whose potential information processing capacity per neuron can only be guessed at, so vast is it) as the “brain of the neuron”. Christof’s suggestion for producing qualia is neurons whose axons reverberate via cell bodies, bypassing dendrites altogether.

Two more quibbles: First, Christof describes how he once thought that understanding anesthesia would be useful in understanding consciousness, but became disillusioned. The dismay stems from two major points: a) a variety of types of molecules/drugs are used to produce anesthesia, and b) anesthetics act on a variety of brain proteins. Christof concludes anesthetics are “too blunt a tool” to discern the site of consciousness. I disagree. While various types of drug molecules are used in anesthesia, the volatile, inhaled gas anesthetics are by and large the only true, complete anesthetics. As opposed to a smorgasbord of drugs, anesthetic gases by themselves erase consciousness (though typically we do add others). Anesthetic gases include a variety of types of molecules: halogenated hydrocarbons, ethers, the inert elemental gas xenon, nitrous oxide etc. And they act on a host of proteins. How to make sense of this morass? It’s been known for a hundred years that anesthetic gases dissolve in a particular non-polar solvent medium, characteristic of olive oil (in fact anesthetic potency correlates with this solubility). This oily solubility medium is found in discrete “hydrophobic pockets” of certain brain proteins. The tiny pockets (~ 1/50 the volume of the protein) act as “the brain of the protein” because subtle (quantum mechanical) forces among intra-pocket electrons (e.g. from benzene-like rings in certain amino acids) control the protein’s conformational state (e.g. channel open or closed). Anesthetics get into the pockets and form their own quantum forces, thereby preventing the conformational activities.

Here’s the rub. At just the right anesthetic concentration, by and large ONLY consciousness is inhibited. Other brain activities (and bodily functions) are unaffected. Thus only proteins required for consciousness have critical hydrophobic pockets (or depend on subtle electron movements within them for function). So the site of action of anesthesia, and the site of consciousness, is not a specific brain location or type of neuron or particular protein. The site/action of anesthesia and consciousness is a distributed phase of non-polar, hydrophobic solubility medium composed of discrete pockets in a group of proteins throughout the brain. In this hydrophobic phase, quantum mechanical forces rule. Which leads to my next quibble. Christof dispenses with the Penrose-Hameroff quantum consciousness microtubule model early on (page 7 to be exact). According to Christof, Penrose-Hameroff is dead-on-arrival because of “the lack of any biophysical mechanism that would permit neurons, and not just any cells in the body, to rapidly form highly specific coalitions across large regions of the brain on the basis of quantum-coherency effects”. Well, gap junction networks with a hydrophobic phase describe just such a mechanism (and only in the brain), assuming quantum coherence can be sustained in one neuron. That brings us to Christof’s second point: “All this is supposed to take place…at body temperature, a rather hostile environment for sustaining quantum coherency over macroscopic scales. See Grush and Churchland (1995) for a telling criticism.”

It turns out that quantum coherence in some circumstances flourishes at high temperature (in which the coherence is pumped, rather than condensed by cooling). A laser is a longstanding example, and recent evidence shows that organic benzene molecules (identical to those in hydrophobic pockets of brain proteins) mediate quantum states more efficiently at high temperatures, and that noise can enhance quantum processes. Physicists Scott Hagan, Jack Tuszynski and I have shown how biophysical mechanisms (e.g. actin gelation, Debye screening) can sustain quantum coherent superposition in microtubules for hundreds of milliseconds. As for Grush and Churchland, their objections were answered tit-for-tat in an article by Roger Penrose and me in the subsequent issue of the journal in which their attack appeared (many quote the attack; few read the rebuttal). Quantum computation in microtubules is not proven, but it hasn’t been refuted. And unlike other theories, it is falsifiable and actually addresses the hard problem.

Let’s get back to Christof’s book. He’s bet the farm on spikes, and there’s no evidence to support the notion that spikes alone generate consciousness. Every instance of correlation between spikes and consciousness also includes dendritic activities. On the other hand there are reasons to believe (40 Hz, computational processing, dendro-dendritic interactions, post-synaptic site of anesthetic effect) that dendritic activities do generate consciousness. Perhaps quantum computations in microtubules in dendrites linked by gap junctions generate consciousness. But even if not, dendrites are in some way involved. The Quest for Consciousness is heading in the wrong direction.

(2) Koch Response to Hameroff

Article, [SCR 2004, December, No. 2]

In Stuart Hameroff’s review of my book, The Quest for Consciousness: A Neurobiological Approach, he praises many attributes of its empirical program to explore the neural basis of consciousness that the late Francis Crick and I have been advocating for years. Stuart also cites instances where he and I differ as to which evidence to favor and what seems reasonable or not in the search for the material roots and causes of consciousness. This is fair enough. However, there are three specific points in Stuart’s essay that do not give a correct reading of the extant data. Let me address these.

Gap junctions and consciousness
As Stuart correctly points out, a flurry of studies over the last handful years have shown that electrical gap junctions play a much larger role in cortex than previously realized (for a review, see Bennett and Zuki, 2004). The focus has been on gap junctions mediated by the Connexin family of proteins (which has at least 10 members expressed in the mammalian central nervous system); they provide a low-resistance, electrical pathway between two neurons –– hence their common alias, electrical synapses. The most important connexin of the adult brain is Cx36. These proteins link groups of local, inhibitory interneurons into large networks (forming a “hyperneuron”), restricted to specific layers in neocortex and hippocampus. Different from their conventional chemical synapses that would serve to inhibit the firing activity of their postsynaptic targets, gap junctions can cause the membrane depolarization in one interneuron to spread to others. This has given rise to the hypothesis that Cx36 gap junctions synchronize the firing of these interneurons, enabling the entire population to fire in lock step in the 30-70 Hz (gamma) range. If such synchronized and rhythmic firing is important for certain aspects of attention, perception and consciousness, then mice that lack gap junctions should show major deficits. It has been possible to breed mice that lack the gene for the Cx35 protein. In these knockout mice, interneuron coupling is greatly reduced; this goes hand-in-hand with a loss of spike synchrony among them (however, gamma range oscillation persist, albeit at a reduced amplitude). The animals have decreased retinal function at low light levels (as expected from a loss of gap junctions in the retina) and reduced reproductive rates, but otherwise no major behavioral deficiencies; they display no obvious loss of motor coordination, and can stay on a rotating cylinder (rotorod test) as well as normal, wildtype mice. By and large, the Cx36 knockout mice have a relatively benign phenotype. Of course, it is quite possible that the behavioral assays used so far are too crude to detect perceptual pathologies or other deficits in rodent consciousness. For example, it may be possible that these mice can be conditioned using aversive delay, associative (Pavlovian) conditioning but not using the more sophisticated form of trace conditioning (in which there is an interval between the end of the tone and the onset of the foot shock (Han et al., 2003).

The idea that the firing activity of groups of interneurons, possibly extending over several cortical columns, is tightly synchronized and may underlie the coalitions of neurons that are sufficient for any one conscious percept is a fascinating one to me. However, no positive evidence links neuron-to-neuron coupling in cortex via gap junctions to perception, let alone consciousness. Thus, the cautionary statement in my book, “ Not enough is known about this phenomenon to implicate it in conscious perception.” remains true today. This may always change in the future, of course.

Dendrites and consciousness

Stuart criticizes my neglect of dendrites, the extended appendages formed by all nerve cells and that carry the majority of synapses. He states his opinion flat out as “Consciousness occurs in dendrites, and the results are conveyed elsewhere by axonal spikes.

I do not understand this statement. Does he mean to imply that the dendritic tree of any one neuron is sufficient for consciousness? Or that dendrites, collectively, are essential to understanding the neuronal correlates of consciousness? Furthermore, I have never stated “that axons reverberate via cell bodies, bypassing dendrites altogether”. In my PhD thesis, I modeled nonlinear computations occurring in the dendritic trees of retinal ganglion cells. I am the author of a textbook “Biophysics of Computation: Information Processing in Single Neurons” (Oxford University Press, 1999) whose topic is the large repertoire of mathematical operations available to single neurons, implemented by voltage- and ligand-dependent channels, and particular synaptic architectures coupled to complex dendritic tree morphology.

In 2002, we published empirical evidence in Nature that a single neuron in the locust’s visual system multiplies its two inputs within its dendritic tree (Gabbiani et al., 2002). Finally, in footnote 22 of Chapter 15, I point out a specific coincidence-detection mechanism within the apical tuft of large, layer 5 pyramidal neurons in neocortex. This operation might be the crucial ingredient for feedback from the front of the cortex to its back that is, so I argue, an essential requirement for the NCC. I don’t discuss these ideas in more depth given 1) our lack of knowledge (by-and-large, dendritic trees of cortical neurons remain offlimit to the intrusive inspection by intracellular electrodes in behaving animals) and 2) our extremely limited ability at this point in time to interfere in a delicate, deliberate, reversible and transient manner with dendritic mechanisms under in vivo conditions. What is needed are not general statements about the importance of dendrites – clearly dendritic trees are an integral part of the nervous system and the brain wouldn’t work without them – but specific, biophysically plausible, proposals.

The action of anesthesia
Stuart disagrees with my statement that “So far, they [i.e. anesthetics] have proven to be too blunt of a tool to help in our quest, though that may change in the future. “ (p. 96), in particular as applied to volatile, inhaled gas anesthetics (e.g., ether, nitrous oxide).

All of the recent evidence implicate specific proteins, in particular voltage- and ligand-gated ionic protein channels as the site action of such volatile agents (e.g. Sonner et al., 2003). This does not rule out that some anesthetics may exert some of their diverse effects in a global, unspecific manner, compatible with the Meyer-Overton lipid solubility relationship (see, for example, Tang and Xu, 2002). Whether or not quantum mechanical effects play any role at all in their action, as asserted by Stuart, remains speculative.

Stuart claims that at just the right concentration, gas anesthetics only inhibit consciousness. This is news to me. More than one hundred years of experience has shown that the majority of anesthetic agents act in a dose-dependent manner, first causing analgesia, then amnesia, followed by loss of purposeful response, immobility and finally autonomic stability. Somewhere along this concentration gradient consciousness begins to be progressively reduced until it is finally abolished. At any given therapeutic concentration, a host of bodily processes is affected (e.g. cardiac or pulmonary function). The discovery of an agent that would turn consciousness off and back on again, without affecting other brain and body functions, would revolutionize the practice of anesthesiology and the study of the neuronal roots of consciousness. Unfortunately, to the best of my knowledge, no such substance exists today. As I noted in my book, one attractive spin-off of discovering the neuronal correlates of consciousness would be the design of such substances. This, I challenge Stuart to provide evidence of loss of consciousness without concomitant loss of pain perception, memory impairment, pulmonary function and so on.

November 2004: Vol 2: Heading in the wrong direction: Review of Christof Koch's "The quest for consciousness" by Stuart Hameroff. This link is broken please see Hameroff's Review at the top of this page.

(3) Hameroff's response to Koch (January 3, 2005):

Pointing the quest in the proper direction

Thanks to Christof Koch for his response to my critique of his book “The quest for consciousness”. I believe this type of debate is quite useful, and take the opportunity here to reply to the three major points he raised.

HAMEROFF'S RESPONSE

1) Gap junction hyper-neurons

Stuart: Regarding my suggestion that gap junction-connected neurons (“hyper-neurons”) may be the neural correlate of consciousness, Christof raises the issue of connexin-36 (a brain gap junction protein) knockout mice who appear relatively normal from a cognitive standpoint, and are presumably conscious. (This exact point was debated on PSYCHE-B a year or so ago, raised by Johnjoe MacFadden). Christof notes that gamma synchrony continued in the knockout mice, though reduced.

As Christof notes, there at least ten types of connexins. Additional connexins are being discovered all the time. Further, another family of gap junction proteins – the pannexins – has been uncovered. So when Christof says: “The most important connexin of the adult brain is Cx36”, this is not necessarily the case. And to say that connexin-36 knockout mice lack functional gap junctions in their brains is an extremely weak contention (e.g. shown by the occurrence of even weak gamma synchrony).

Christof: “Stuart criticizes my neglect of dendrites, the extended appendages formed by all nerve cells and that carry the majority of synapses. He states his opinion flat out as “Consciousness occurs in dendrites, and the results are conveyed elsewhere by axonal spikes. I do not understand this statement. Does he mean to imply that the dendritic tree of any one neuron is sufficient for consciousness? Or that dendrites, collectively, are essential to understanding the neuronal correlates of consciousness?

Stuart: My statement implies that the collective dendritic tree of a hyper-neuron - a set of neurons linked by dendro-dendritic gap junctions - is essential to understanding the neuronal correlate of consciousness. This may include the dendrites of tens of thousands or more individual neurons. Because gap junctions change dynamically, a different particular (Hebbian) hyper-neuron set of dendrites can be the NCC at any one time, each lasting, say, hundreds of milliseconds.

On page 103 in Chapter 5 (“What are the neuronal correlates of consciousness”) of The quest for consciousness, Christof states: “I therefore look for particular mechanisms that confer onto coalitions of neurons properties that correspond to attributes of conscious percepts. One possibility might be small sets of cortical pyramidal cells that receive strong excitatory synaptic input from another set of pyramidal cells directly onto their cell bodies in a reciprocal manner. Such an arrangement might instantiate a loop, a set of neurons that, once triggered, would keep on firing until actively inhibited by another coalition of neurons. The firing dynamics of such a group might be close to that of consciousness…”

3) The action of anesthesia

Christof: Stuart disagrees with my statement that “So far, they [i.e. anesthetics] have proven to be too blunt of a tool to help in our quest, though that may change in the future. “ (p. 96), in particular as applied to volatile, inhaled gas anesthetics (e.g., ether, nitrous oxide). All of the recent evidence implicate specific proteins, in particular voltage- and ligand-gated ionic protein channels as the site action of such volatile agents (e.g. Sonner et al., 2003). This does not rule out that some anesthetics may exert some of their diverse effects in a global, unspecific manner, compatible with the Meyer-Overton lipid solubility relationship (see, for example, Tang and Xu, 2002). Whether or not quantum mechanical effects play any role at all in their action, as asserted by Stuart, remains speculative.

Stuart: I agree completely that sets of specific proteins mediate anesthetic effects. (But in addition to membrane proteins, dont forget the cytoskeleton. Both actin and microtubules are affected.) Sets of specific proteins means that numerous proteins mediate effects of any one gas anesthetic. At first glance this seems like ”too blunt a tool”. But anesthetics act on proteins precisely according to the Meyer-Overton lipid solubility relationship. All proteins affected by gas anesthetics (and thus proteins which mediate consciousness) have lipid-like (”hydrophobic”) pockets within them, where anesthetics act. And they bind in these pockets by Van der Waals London forces which are quantum effects. This is not speculation. It is also not speculation that (in the absence of anesthetics, i.e. during consciousness) quantum London forces in hydrophobic pockets can regulate conformational dynamics of certain proteins. What is speculation is that, by forming their own London forces in the pockets, the anesthetics are disturbing normally occurring London forces necessary for protein function and consciousness. It is also speculation that quantum states in hydrophobic pockets form (near) brain-wide macroscopic quantum states through coherence/entanglement/condensation. But these speculations are falsifiable, and generate testable predictions.

Christof: Stuart claims that at just the right concentration, gas anesthetics only inhibit consciousness. This is news to me. More than one hundred years of experience has shown that the majority of anesthetic agents act in a dose-dependent manner, first causing analgesia, then amnesia, followed by loss of purposeful response, immobility and finally autonomic stability.

Stuart: (I’ve only been practicing anesthesiology for 30 years.) But what Christof is correctly describing is the well known four stages of ether anesthesia discovered in the last century (except Christof left out an excitatory phase between loss of purposeful response and immobility). Autonomic [in]stability is below the level of anesthesia. By and large these stages still hold true for modern gas anesthetics.

Christof: Somewhere along this concentration gradient consciousness begins to be progressively reduced until it is finally abolished.

Stuart: I agree that ”somwhere along this concentration gradient” consciousness is lost. But how do you know consciousness is progressively reduced? How do you know it doesnt cease abruptly underneath the unconscious behaviors you describe?

Christof: At any given therapeutic concentration, a host of bodily processes is affected (e.g. cardiac or pulmonary function).

Stuart: (I said ”by and large” only consciousness is affected.) For any single patient there is precisely one therapeutic concentration. But finding the precise therapeutic concentration – just enough to erase consciousness with minimal side effects - is sometimes a bit tricky (for one thing, it changes during an anesthetic for various reasons, e.g. temperature). So we tend to err on the side of slightly too much anesthetic to avoid awareness. But at just the right anesthetic amount, amazingly few bodily processes are affected (and the extent depends on a host of factors like hydration, and intrinsic organ function etc.). Plus, consciousness includes putting out various hormones like catecholamines (e.g. adrenaline) which are not put out during anesthesia.

Christof: I challenge Stuart to provide evidence of loss of consciousness without concomitant loss of pain perception, memory impairment, pulmonary function and so on.

Stuart: OK.

Pain perception: Patients under anesthesia may respond to pain with autonomic changes in blood pressure, heart rate, pupillary size, lacrimation, sweating, mucous secretion etc. Pain from tourniquets placed on arms or legs (to reduce blood flow in the surgical field) cause increases in blood pressure and heart rate. As anesthesiologists, we use these autonomic signs as early warnings to deepen the anesthetic level. They are nonconscious responses.

Patients under anesthesia also have relatively intact sensory evoked potentials, and visual evoked potentials (auditory evoked potentials are the most sensitive to anesthetic effect).

Memory: Numerous studies have shown that implicit learning/memory occurs under anesthesia. Phil Merikle, for example, did such studies years ago. (Phil, however, put the nonconscious pain responses noted above together with the implicit learning and occasional reports of awareness under anesthesia to suggest – incorrectly in my view – that patients do not lose consciousness under anesthesia, they just suffer and don’t remember. There are many arguments against this idea, but because consciousness is unmeasurable it is impossible to completely refute. But it is also impossible to prove that anyone other than one’s self is conscious.)

Pulmonary function: Anesthetized patients routinely breathe on their own during general anesthesia. The gas anesthetics shift the slope of the carbon dioxide response curve somewhat (we breathe in response to carbon dioxide), and slightly impair ciliary function (cilia are made of microtubules, and act to expel mucous etc. from the lungs). But breathing is relatively unaffected at therapeutic concentration (unless we add muscle paralyzing agents of course, in which case breathing stops entirely).

Christof: The discovery of an agent that would turn consciousness off and back on again, without affecting other brain and body functions, would revolutionize the practice of anesthesiology and the study of the neuronal roots of consciousness.

Stuart: We basically have that now: the gas anesthetics. They are not perfect, but close.

The problem is that Christof (like most people in the anesthetic mechanism field) is operating from the assumption that consciousness involves a specific set of neurons, a specific type of receptor, a specific type of circuit. That’s what they are looking for and its not there. The answer is right in front of us. As I said in my review:

”...the site of action of anesthesia, and the site of consciousness, is not a specific brain location or type of neuron or particular protein. The site/action of anesthesia and consciousness is a distributed phase of non-polar, hydrophobic solubility medium composed of discrete pockets in a group of proteins throughout the brain. In this hydrophobic phase, quantum mechanical forces rule.”

In my opinion, consciousness happens in quantum pockets in hyper-neuron dendrite proteins. That is where the evidence points. That is where the quest for consciousness should be looking.